Myricitrin inhibits vascular adhesion molecule expression in TNF‑α‑stimulated vascular smooth muscle cells

Mol Med Rep. 2017 Nov;16(5):6354-6359. doi: 10.3892/mmr.2017.7321. Epub 2017 Aug 22.

Abstract

Increased expression of adhesion molecules is thought to serve an important role in the pathogenesis of atherosclerosis. Myricitrin, a bioactive compound of Myrica cerifera, has been demonstrated to exhibit anti‑atherogenic effects. However, the effect of myricitrin on the expression of adhesion molecules in vascular smooth muscle cells (VSMCs) remains unknown. Therefore, the aim of the present study was to evaluate the inhibitory effects of myricitrin on tumor necrosis factor‑α (TNF‑α)‑induced expression of adhesion molecules in VSMCs in vitro. The results revealed that myricitrin inhibited the adhesion of human THP‑1 monocyte cells to TNF‑α‑stimulated mouse MOVAS‑1 VSMC cells, and reduced the expression of adhesion molecules in TNF‑α‑stimulated MOVAS‑1 cells. In addition, myricitrin significantly inhibited the TNF‑α‑induced expression of nuclear factor (NF)‑κB p65, and prevented the TNF‑α‑induced degradation of nuclear factor of κ light chain enhancer in B‑cells inhibitor α. Furthermore, myricitrin inhibited the production of intracellular reactive oxygen species in TNF‑α‑stimulated MOVAS‑1 cells. In conclusion, the results of the present study indicated that myricitrin inhibits the expression of vascular cell adhesion protein‑1 and intercellular adhesion molecule‑1 in TNF‑α‑stimulated MOVAS‑1 cells potentially via the NF‑κB signaling pathway. Therefore, myricitrin may be an effective pharmacological agent for the prevention or treatment of atherosclerosis.

MeSH terms

  • Animals
  • Antioxidants / pharmacology*
  • Cardiovascular Agents / pharmacology*
  • Cell Line
  • Flavonoids / pharmacology*
  • Gene Expression Regulation
  • Humans
  • Intercellular Adhesion Molecule-1 / genetics*
  • Intercellular Adhesion Molecule-1 / metabolism
  • Mice
  • Muscle, Smooth, Vascular / cytology
  • Muscle, Smooth, Vascular / drug effects
  • Muscle, Smooth, Vascular / metabolism
  • Myocytes, Smooth Muscle / cytology
  • Myocytes, Smooth Muscle / drug effects*
  • Myocytes, Smooth Muscle / metabolism
  • Myrica / chemistry
  • NF-KappaB Inhibitor alpha / genetics
  • NF-KappaB Inhibitor alpha / metabolism
  • Reactive Oxygen Species / antagonists & inhibitors
  • Reactive Oxygen Species / metabolism
  • Signal Transduction
  • THP-1 Cells
  • Transcription Factor RelA / genetics
  • Transcription Factor RelA / metabolism
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors*
  • Tumor Necrosis Factor-alpha / pharmacology
  • Vascular Cell Adhesion Molecule-1 / antagonists & inhibitors
  • Vascular Cell Adhesion Molecule-1 / genetics*
  • Vascular Cell Adhesion Molecule-1 / metabolism

Substances

  • Antioxidants
  • Cardiovascular Agents
  • Flavonoids
  • Reactive Oxygen Species
  • Rela protein, mouse
  • Transcription Factor RelA
  • Tumor Necrosis Factor-alpha
  • Vascular Cell Adhesion Molecule-1
  • Intercellular Adhesion Molecule-1
  • NF-KappaB Inhibitor alpha
  • myricitrin